Ce diaporama a bien été signalé.
Nous utilisons votre profil LinkedIn et vos données d’activité pour vous proposer des publicités personnalisées et pertinentes. Vous pouvez changer vos préférences de publicités à tout moment.
Charcot Foot
Miss Sheweidin Aziz – ST3 T&O
Boston Pilgrim Hospital
June 2016
HISTORY
• In 1703 William Musgrave first described a neuropathic joint
as an arthralgia caused by venereal disease
• In 18...
DEFINITION
• Neuropathic (Charcot) osteoarthropathy is a non infective,
destructive, lesion of a bone and joint resulting ...
• A chronic and progressive joint disease following loss of
protective sensation and leads to destruction of joints and
su...
RISK FACTORS
• Diabetic neuropathy
• Alcoholism
• Leprosy
• Meningomyelocele
• Tabes dorsalis/syphilis
• Syringomyelia
• A...
EPIDEMIOLOGY
• In diabetic patients: 0.1-1.4%
• In diabetics with neuropathy 7.5%
• Bilateral disease occurs in <10%
• Typ...
PATHOPHYSIOLOGY
Neurotraumatic theory: German theory 1946
• Peripheral neuropathy  loss of protective sensation 
increas...
PATHOPHYSIOLOGY
Neurovascular theory: French theory 1868
• Spinal cord lesion  autonomic neuropathy  AV shunting
 incre...
PATHOPHYSIOLOGY
Molecular biology
• Inflammatory cytokines may cause destruction IL-1 and TNF
– alpha  increased producti...
CLINICAL PRESENTATION
• Symptoms
• Swelling foot and ankle
• Pain 50%
• Loss of function
CLINICAL PRESENTATION
• Acute Charcot
• Swelling
• Warmth (3.3° warmer)
• Erythema (will decrease with Charcot but not wit...
CLINICAL PRESENTATION
• Chronic Charcot
• Structurally deformed foot
• Rocker bottom deformity
• Collapsed medial arch
CLASSIFICATION
Stage 0: Joint oedema. Negative radiographs.
Stage 1: Fragmentation. Joint oedema. Bone
resorption. Dislocations. Fractures
Stage 2: Coalescence. Decreased local oedema.
Sclerosis. Fracture healing. Debris resorption.
Decreased joint mobility.
Stage 3: Reconstruction. No joint oedema.
Consolidation and remodelling of fracture
fragments. Ulcers may develop.
INVESTIGATION
• Inflammatory markers: Elevated in Osteomyelitis and
Charcot
• Bone scan: useful in presence of superimpose...
• MRI: differentiate between abscess and soft tissue swelling
• Biopsy: to guide antibiotic therapy
• Histology: Synovial ...
MANAGEMENT
• Non-operative
• Total contact casting every 2-4 weeks for 2-4 months
• Orthotics – Charcot restraint orthotic...
• Operative
• Resection of bony prominences (exostectomy) and
Achilles Tendon lengthening
• Braceable foot with equinus de...
• Deformity correction, arthrodesis +/- osteotomy
• Severe deformity that is not braceable
• High complication rate up to ...
Sohn et al performed a retrospective study to compare the risks of
lower-extremity amputation
• Charcot patients had a 4.1...
THANK YOU
Charcot foot
Charcot foot
Prochain SlideShare
Chargement dans…5
×

Charcot foot

3 023 vues

Publié le

General overview. Good starting point.

Publié dans : Santé & Médecine
  • Soyez le premier à commenter

Charcot foot

  1. 1. Charcot Foot Miss Sheweidin Aziz – ST3 T&O Boston Pilgrim Hospital June 2016
  2. 2. HISTORY • In 1703 William Musgrave first described a neuropathic joint as an arthralgia caused by venereal disease • In 1868 Jean-Martin Charcot gave the first detailed description of the neuropathic aspect. He noted this disease process as a complication of syphilis (most common cause until 1936 when Jordan linked it to Diabetes)
  3. 3. DEFINITION • Neuropathic (Charcot) osteoarthropathy is a non infective, destructive, lesion of a bone and joint resulting from a fracture or dislocation or both in a patient who has peripheral neuropathy
  4. 4. • A chronic and progressive joint disease following loss of protective sensation and leads to destruction of joints and surrounding bony structures. May lead to amputation if left untreated
  5. 5. RISK FACTORS • Diabetic neuropathy • Alcoholism • Leprosy • Meningomyelocele • Tabes dorsalis/syphilis • Syringomyelia • Any condition that causes sensory or autonomic neuropathy
  6. 6. EPIDEMIOLOGY • In diabetic patients: 0.1-1.4% • In diabetics with neuropathy 7.5% • Bilateral disease occurs in <10% • Type 1 DM: 20-25 years post diagnosis • Type 2 DM: 5-10 years post diagnosis • Gender ?Male predominance
  7. 7. PATHOPHYSIOLOGY Neurotraumatic theory: German theory 1946 • Peripheral neuropathy  loss of protective sensation  increase susceptibility to injuries (repeated minor or acute)  progressive destruction and damage to bone and joints
  8. 8. PATHOPHYSIOLOGY Neurovascular theory: French theory 1868 • Spinal cord lesion  autonomic neuropathy  AV shunting  increased blood flow (warm foot and dilated veins)  Increased osteoclast activity  bone resorption and mechanical weakening  fractures and deformity
  9. 9. PATHOPHYSIOLOGY Molecular biology • Inflammatory cytokines may cause destruction IL-1 and TNF – alpha  increased production of transcription factor - kB
  10. 10. CLINICAL PRESENTATION • Symptoms • Swelling foot and ankle • Pain 50% • Loss of function
  11. 11. CLINICAL PRESENTATION • Acute Charcot • Swelling • Warmth (3.3° warmer) • Erythema (will decrease with Charcot but not with infection on elevation)
  12. 12. CLINICAL PRESENTATION • Chronic Charcot • Structurally deformed foot • Rocker bottom deformity • Collapsed medial arch
  13. 13. CLASSIFICATION
  14. 14. Stage 0: Joint oedema. Negative radiographs.
  15. 15. Stage 1: Fragmentation. Joint oedema. Bone resorption. Dislocations. Fractures
  16. 16. Stage 2: Coalescence. Decreased local oedema. Sclerosis. Fracture healing. Debris resorption. Decreased joint mobility.
  17. 17. Stage 3: Reconstruction. No joint oedema. Consolidation and remodelling of fracture fragments. Ulcers may develop.
  18. 18. INVESTIGATION • Inflammatory markers: Elevated in Osteomyelitis and Charcot • Bone scan: useful in presence of superimposed osteomyelitis • Technetium bone scan: maybe positive in infection or Charcot • Indium WBC scan: Negative in Charcot. Positive in osteomyelitis
  19. 19. • MRI: differentiate between abscess and soft tissue swelling • Biopsy: to guide antibiotic therapy • Histology: Synovial hypertrophy and detritic synovitis
  20. 20. MANAGEMENT • Non-operative • Total contact casting every 2-4 weeks for 2-4 months • Orthotics – Charcot restraint orthotics walker (CROW) boot can be used after TCC • Shoe modifications to reduce ulcerations
  21. 21. • Operative • Resection of bony prominences (exostectomy) and Achilles Tendon lengthening • Braceable foot with equinus deformity and focal bony prominence causing skin breakdown • Aim to achieve plantigrade foot that allows ambulation without skin compromise
  22. 22. • Deformity correction, arthrodesis +/- osteotomy • Severe deformity that is not braceable • High complication rate up to 70% • Amputation • Failed surgery. Unstable arthrodesis. Recurrent infection • Aim is for partial or limited amputation if vascularity allows
  23. 23. Sohn et al performed a retrospective study to compare the risks of lower-extremity amputation • Charcot patients had a 4.1 amputations per 100 person-years vs ulcer patients 4.7 • In patients under 65 years amputation risk 7x in ulcer only vs. 12x for Charcot and ulcer
  24. 24. THANK YOU

×